Vascular attack as a therapeutic strategy for cancer.
The blood supply to all solid tumours consists of parasitized normal vessels and new vessels which have been induced to grow by the presence of the tumour. These vessels are inadequate in many respects, being tortuous, thin-walled, chaotically arranged, lacking innervation and with no predetermined direction of flow. The walls consist of a basement membrane lined with rapidly proliferating immature endothelial cells, and are more permeable than normal vessels. The spacing of the vessels and their average diameters are not optimal for nutrient provision. This paper focuses on the evidence that many existing therapies may already have, as part of their action, a vascular mediated process of killing tumour cells. This may result from local changes within individual vessels or from systemic alterations in blood pressure, viscosity, coagulability etc. The hallmarks of vascular injury are identified and the dangers of discarding useful anticancer agent by failing to understand their mechanism of action are highlighted.
Denekamp
J
J
CRC Gray Laboratory, Mount Vernon Hospital, Northwood, Middlesex, UK.
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D001808:Blood Vessels / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D006979:Hyperthermia, Induced; D009369:Neoplasms / Q000098:blood supply* / Q000628:therapy*
D000970:Antineoplastic Agents